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PubMed1985

Chromosomes of G2 arrested cells are easily analyzed by use of the 'tsBN2' mutation.

The tsBN2 cell line, a temperature sensitive (ts) mutant of the BHK21/13 cell line (Nishimoto, T. et al. Somatic Cell Genet. 4, 323-340, 1978) has a ts defect in its regulatory mechanism for the initiation of chromosome condensation, the so-called, premature chromosome condensation (PCC) being induced at a nonpermissive temperature (Nishimoto, T. et al. Cell 15, 475-483, 1978, Nishimoto, T. et al. J. Cell Physiol. 109, 299-308, 1981). Using the 'tsBN2' mutation, we analyzed chromosomes of tsBN2 cells arrested in the G2 phase with neocarzinostatin (NCS) and found considerable aberrations, such as gaps, breaks and double minutes-like fragmentation, in addition to a typical G2-chromosome (a long filamental chromosome made up of two chromatids). Our results provide evidences that the tsBN2 cell line can be used for examinations of the chromosomes of cells arrested in the G2 phase.

Animals↗
PubMed1982

[Kinetic study of cell proliferation in the amphibian thymus. Relationship to histological differentiation].

Cell proliferation kinetics were investigated in the thymus of the newt Pleurodeles waltlii during larval life and metamorphosis. Cell cycles lengthened continuously, particularly G1 and G2 phases. Relative durations of G1 and G2 (differentiation phases) lengthened, while relative durations of S and M (multiplication phases) shortened. Consequently, multiplication rate decreased regularly. Mitotic index, labelling index and growth fraction increase up to stage 50, then decreased markedly. Stage 50 is an important one, as cell cycles duration and growth fraction vary inversely from this point onwards; it marks the end of the period of intense proliferation and rapid growth of the thymus, and also the beginning of the period during which all differentiated cell types are present, cell proliferation decreasing and becoming markedly diminished after the end of metamorphosis.

Animals↗
PubMed1985

Cell proliferation during postnatal development of the retina in the mouse.

Cell proliferation was studied in the developing mouse retina by autoradiography following injection of [3H]thymidine. In 1-day-old mice, the duration of the phases of the cell-division cycle was investigated in ventricular cells, the mitotically active precursors of postmitotic cells that comprise the neural retina. In the center of the retina, the generation time (T) was 30 h, consisting of 8.5 h G1 phase, 16.0 h S phase, 2.6 h (minimum) G2 phase, and 2.5 h mitosis. In the periphery, T was 28.5 h; G1, 7.5 h; S, 16.0 h; minimum G2, 2.6 h; and mitosis, 2 h. As embryogenesis proceeds, the mitotic cycle decelerates. In contrast with postembryonic cell populations (in which G2, S and M tend to be invariable), all phases of the cycle increase in duration, and most become longer than is commonly observed in mature animals. Approx. 18 generations of ventricular cells are produced. However, throughout the stage of multiplication, some cells cease dividing and differentiate. In 1-day-old mice, 23% of ventricular cells in the center of the retina and 37% in the periphery remain mitotically active. DNA synthesis ceases on the 6th day in the center and the 11th day in the periphery.

Animals↗
PubMed1994

IL-2-induced expression of TTK, a serine, threonine, tyrosine kinase, correlates with cell cycle progression.

We have recently isolated the cDNA for a unique human 97-kDa kinase, TTK, by expression screening of a cDNA expression library using anti-phosphotyrosine antibodies. When expressed in Escherichia coli, TTK can phosphorylate serine, threonine, and tyrosine residues. Thus TTK appears to belong to a newly described family of kinases able to phosphorylate all three hydroxy amino acids. This family of multispecific kinases includes several other kinases involved in cell cycle progression. In support of a possible role in regulating cell cycle progression, TTK message is readily detected in rapidly proliferating tissues in vivo including testes, thymus, bone marrow, and many malignant tumors, but not in benign tissues with a low proliferative rate in vivo. To determine the effect of cell activation and cell cycle progression on TTK expression, we measured TTK mRNA and protein levels as well as kinase activity in freshly isolated T cells or IL-2-expanded T cell blasts activated to proliferate by the addition of a variety of mitogens. TTK mRNA levels, protein levels, and kinase activity were greatly enhanced when either freshly isolated PBL or T cell blasts were activated by cross-linking the TCR complex by mitogenic lectins or by bypassing the TCR with phorbol esters and cation ionophores. Incubation with IL-2 increased TTK expression in PBL blasts, which proliferate in response to IL-2, but not in fresh PBL, which do not proliferate in response to IL-2. TTK expression was blocked by either cyclosporin A or FK520, which inhibit IL-2 production and could be recovered by the addition of exogenous IL-2. Furthermore, TTK expression was prevented by incubation of the cells with rapamycin, which blocks IL-2 signaling. Thus, TTK expression in T cells appears to be a consequence of IL2-induced cell proliferation. Agonist-induced TTK expression was a delayed event occurring 12 to 24 h after activation of PBL blasts and 48 to 72 h after activation of fresh PBL. TTK protein and mRNA expression increased in both fresh PBL and T cell blasts concurrently with passage of cells through S phase as indicated by [3H]TdR incorporation and cell cycle analysis of propidium iodide-stained cells. TTK mRNA and protein levels reached a maximum as cells entered the G2 phase of the cell cycle. These results were confirmed by cell cycle blockade studies with aphidicolin and nocodazole wherein TTK protein levels are not detected in cells in G1 and are readily detectable in cells in the S and G2 phases of the cell cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

CD3 Complex↗
PubMed1978

Messenger RNA synthesis in synchronized Chinese hamster ovary cells.

Chinese hamster ovary cells were synchronized without inhibitors by mitotic selection and labelled in G1, S or G2 phase by incubation for 90 min with [3H]- OR [14C]uridine. Purified polyribosomes were extracted with phenol and the polyadenylated mRNA prepared by poly(U)-Sepharose chromatography. Poly-adenylated [3H]uridine-labelled mRNA from the G1 phase of the cell cycle was compared by exponential polyacrylamide gel electrophoresis in formamide with [14C] uridine-labelled polyadenylated nRNA from the S or G2 phase. The electrophoretic patterns obtained correspond to the size range expected for mRNA (7-28 S). No prominent differences were detected between mRNAs synthesized in different phases of the cell cycle. From these data we conclude that the major size classes of polyribosomal poly(A)-containing mRNA are synthesized in equal ratios throughout the cell cycle.

Cell Cycle↗
PubMed1995

Cell cycle regulation of RNA polymerase III transcription.

Inactivation of the TATA-binding protein-containing complex TFIIIB contributes to the mitotic repression of RNA polymerase III transcription, both in frogs and in humans (J. M. Gottesfeld, V. J. Wolf, T. Dang, D. J. Forbes, and P. Hartl, Science 263:81-84, 1994; R. J. White, T. M. Gottlieb, C. S. Downes, and S. P. Jackson, Mol. Cell. Biol. 15:1983-1992, 1995). Using extracts of synchronized proliferating HeLa cells, we show that TFIIIB activity remains low during the early part of G1 phase and increases only gradually as cells approach S phase. As a result, the transcription of all class III genes tested is significantly less active in early G1 than it is in S or G2 phase, both in vitro and in vivo. The increased activity of TFIIIB as cells progress through interphase appears to be due to changes in the TATA-binding protein-associated components of this complex. The data suggest that TFIIIB is an important target for the cell cycle regulation of RNA polymerase III transcription during both mitosis and interphase of actively proliferating HeLa cells.

Cell Cycle↗
PubMed2006

Role of mammalian Rad9 in genomic stability and ionizing radiation response.

Eukaryotic cells have evolved DNA damage response mechanisms utilizing proficient DNA repair and cell cycle checkpoints in order to maintain genomic stability. The Schizosaccharomyces pombe Rad9 gene was initially identified as encoding a cell cycle checkpoint protein. When the mammalian homologue of S. pombe Rad9 was inactivated, however, chromosomal instability was observed even in the absence of DNA damaging agents. Both an increase in chromosome end-to-end associations and telomere loss were observed in cells with inactivated mammalian Rad9. This telomere instability correlated with enhanced S- and G2-phase specific cell killing, delayed kinetics of gamma-H2AX foci appearance and disappearance, and reduced chromosomal repair after ionizing radiation (IR) exposure, suggesting that Rad9 plays a role in cell cycle phase specific DNA damage repair. Inactivation of mammalian Rad9 also resulted in decreased homologous recombinational (HR) repair, which occurs predominantly in the S- and G2-phase of the cell cycle. These newly defined functions of mammalian Rad9 are discussed in relation to telomere stability and HR repair as a mechanism for promoting cell survival after IR exposure.

Animals↗
PubMedDate not supplied

[Cytophotometric and biochemical research on the amount of DNA in the nuclei of loach embryos injected with low-molecular RNA].

The cell cycle structure in the cells of loach embryos at the early blastula stage (5 h of development at 21 degrees) is markedly altered under the influence of injection of homologous low molecular weight nuclear RNA and, as a result, the number of cells in G2-phase. The DNA amount in the embryo increases by 20%. At the midblastula stage (7 h) no increase in the number of cells in G2-phase was found.

Animals↗
PubMed1975

Cell cycle dependent agglutinability, distribution of concanavalin A binding sites and surface morphology of normal and transformed fibroblasts.

In studies on phenotypic reversion of transformed cells to normal growth patterns, we investigated the effect of dibutyryl cyclic AMP (dbc-AMP) and a protease inhibitor (TLCK) on growth of SV40-transformed mouse fibroblasts (3T3). The results did not support the hypothesis that transformed cells grown with dbc-AMP or TLCK are induced to contact-mediated growth control. The growth rate of SV-3T3 cells grown with the drugs was strongly reduced, due to accumulation of the cells in the G2 phase of the cell cycle. In addition, decreased agglutinability with concanavalin A (Con A) of those SV-3T3 cells was not caused by a direct effect of the drugs on the cell surface, but by partial synchronization of the cells in the G2 phase of the cycle. In synchronized cultures agglutinability of transformed cells reached a minimum in G2 and was maximal in mitosis and G1. Normal cells agglutinated only in mitosis. This suggested that agglutinability of cells is somehow cell cycle dependent. Cytochemical investigations on normal and transformed 3T3 cells had shown that Con A-induced redistribution of binding sites on the surface of these cells is not correlated with agglutinability. The present work on replicas confirmed this, but indicated also that normal 3T3 cells have more extended lamellipodia with less Con A binding sites than SV-3T3 cells. Preliminary scanning electron microscope data showed cell cycle dependent changes in 3T3 cells and also showed that confluent 3T3 and SV-3T3 cells suspended for agglutination tests had a different surface morphology. These results may represent additional factors important for differences in cell agglutinability by Con A.

Agglutination↗
PubMedDate not supplied

Dinucleoside tetraphosphate variations in cultured tumor cells during their cell cycle and growth.

Asynchronous and synchronized cultures of A549 and HTC cells were used to detect possible, cell cycle or cell density specific variations in the intracellular pools of dinucleoside tetraphosphates (Ap4X). No important variations of the nucleotide pools were observed during cell growth. When HTC cells were released from mitotic arrest, a decrease by a factor of N3 Ap4X and ATP levels was observed when the cells entered the G1 phase. This decrease is essentially due to cell doubling. When A549 cells were released from an arrest at the G1/S boundary, the nucleotide pool size increased slightly during the G2 phase just before mitosis. This result is in agreement with both earlier data from our laboratory and the observed decrease in Ap4X pool after release from mitotic-arrested HTC cells. These results suggest that the Ap4X and ATP pools are only subjected to very small variations during the cell cycle, essentially in the G2 phase and after mitosis.

Adenosine Triphosphate↗
PubMed1995

De novo synthesis of glutathione is required for both entry into and progression through the cell cycle.

To study the putative role of de novo synthesis of glutathione (GSH) in the regulation of the cell cycle, we exposed NIH-3T3 cells to buthionine sulfoximine (BSO) and analysed cell cycle kinetics with continuous bromodeoxyuridine (BrdU) labeling and bivariate Hoechst 33258/ethidium bromide flow cytometry. Treating quiescent cells, which themselves had a low GSH content, with BSO did not affect subsequent entry into and progression through the cell cycle. Adding BSO during serum stimulation, however, provoked a dose-dependent inhibition of cell growth and a delayed increase in GSH level. The cell kinetic mechanism underlying BSO-induced growth inhibition is a diminished entry into the cell cycle and a permanent arrest in the S and G2 phase of the cell cycle. Our results are consistent with the hypothesis that GSH de novo synthesis is required for cell activation and proper S and G2 phase transit.

3T3 Cells↗
PubMed2006

Hedgehog signaling and the retina: insights into the mechanisms controlling the proliferative properties of neural precursors.

Hedgehog signaling has been linked to cell proliferation in a variety of systems; however, its effects on the cell cycle have not been closely studied. In the vertebrate retina, Hedgehog's effects are controversial, with some reports emphasizing increased proliferation and others pointing to a role in cell cycle exit. Here we demonstrate a novel role for Hedgehog signaling in speeding up the cell cycle in the developing retina by reducing the length of G1 and G2 phases. These fast cycling cells tend to exit the cell cycle early. Conversely, retinal progenitors with blocked Hedgehog signaling cycle more slowly, with longer G1 and G2 phases, and remain in the cell cycle longer. Hedgehog may modulate cell cycle kinetics through activation of the key cell cycle activators cyclin D1, cyclin A2, cyclin B1, and cdc25C. These findings support a role for Hedgehog in regulating the conversion from slow cycling stem cells to fast cycling transient amplifying progenitors that are closer to cell cycle exit.

Animals↗
PubMed2002

Radioprotection: the non-steroidal anti-inflammatory drugs (NSAIDs) and prostaglandins.

Clinical and experimental studies of the acute and late effects of radiation on cells have enhanced our knowledge of radiotherapy and have led to the optimisation of radiation treatment schedules and to more precise modes of radiation delivery. However, as both normal and cancerous tissues have similar response to radiation exposure, radiation-induced injury on normal tissues may present either during, or after the completion of, the radiotherapy treatment. Studies on both NSAIDs and prostaglandins have indeed shown some evidence of radioprotection. Both have the potential to increase the survival of cells but by entirely different mechanisms. Studies of cell kinetics reveal that cells in the mitotic (M) and late G2 phases of the cell cycle are generally most sensitive to radiation compared with cells in the early S and G1/G0 phases. Furthermore, radiation leads to a mitotic delay in the cell cycle. Thus, chemical agents that either limit the proportion of cells in the M and G2 phases of the cell cycle or enhance rapid cell growth could in principle be exploited for their potential use as radioprotectors to normal tissue during irradiation. NSAIDs have been shown to exert anti-cancer effects by causing cell-cycle arrest, shifting cells towards a quiescence state (G0/G1). The same mechanism of action was observed in radioprotection of normal tissues. An increase in arachidonic acid concentrations after exposure to NSAIDs also leads to the production of an apoptosis-inducer ceramide. NSAIDs also elevate the level of superoxide dismutase in cells. Activation of heat shock proteins by NSAIDs increases cell survival by alteration of cytokine expression. A role for NSAIDs with respect to inhibition of cellular proliferation possibly by an anti-angiogenesis mechanism has also been suggested. Several in-vivo studies have provided evidence suggesting that NSAIDs may protect normal tissues from radiation injury. Prostaglandins do not regulate the cell cycle, but they do have a variety of effects on cell growth and differentiation. PGE(2) mediates angiogenesis, increasing the supply of oxygen and nutrients, essential for cellular survival and growth. Accordingly, PGE(2) at sufficiently high plasma concentrations enhances cellular survival by inhibiting pro-inflammatory cytokines such as TNF-alpha and IL-1beta. Thus, PGE(2) acts as a modulator, rather than a mediator, of inflammation. Prospective studies have suggested the potential use of misoprostol, a PGE(1) analogue, before irradiation, in prevention of radiation-induced side effects. The current understanding of the pharmacology of NSAIDs and prostaglandins shows great potential to minimise the adverse effects of radiotherapy on normal tissue.

Animals↗
PubMed1988

2-[(Aminopropyl)amino] ethanethiol-mediated reductions in 60Co gamma-ray and fission-spectrum neutron-induced chromosome damage in V79 cells.

The radioprotector 2-[aminopropyl)amino] ethanethiol (WR1065), which has been reported to reduce the cytotoxic and mutagenic effects of low LET radiation, was investigated for its ability to protect against low LET (60Co gamma ray) and high LET (fission-spectrum neutron)-induced chromosome damage in V79 cells. Cells were irradiated in G2 phase in the presence or absence of 4 mM WR1065 and were harvested and analyzed 2 h later for chromatid-type aberrations. Irradiation of G2-phase V79 cells in the presence of WR1065 resulted in a 30 to 50% reduction in the frequency of gamma-ray and neutron-induced chromatid-type breaks and exchanges. The effects were found only after exposures of greater than 200 cGy gamma-ray or 50 cGy neutron irradiation. The radioprotector was effective at reducing neutron-induced aberrations after exposures at dose rates of both 10 and 43 cGy/min. Thus the radioprotector WR1065 is an effective anti-clastogenic agent in V79 cells, protecting against both 60Co gamma-ray and fission-spectrum neutron-induced aberrations, when present during irradiation.

Animals↗
PubMed1980

Cell cycle phase expansion in nitrogen-limited cultures of Saccharomyces cerevisiae.

The time and coordination of cell cycle events were examined in the budding yeast Saccharomyces cerevisiae. Whole-cell autoradiographic techniques and time-lapse photography were used to measure the duration of the S, G1, and G2 phases, and the cell cycle positions of "start" and bud emergence, in cells whose growth rates were determined by the source of nitrogen. It was observed that the G1, S, and G2 phases underwent a proportional expansion with increasing cell cycle length, with the S phase occupying the middle half of the cell cycle. In each growth condition, start appeared to correspond to the G1 phase/S phase boundary. Bud emergence did not occur until mid S phase. These results show that the rate of transit through all phases of the cell cycle can vary considerably when cell cycle length changes. When cells growing at different rates were arrested in G1, the following synchronous S phase were of the duration expected from the length of S in each asynchronous population. Cells transferred from a poor nitrogen source to a good one after arrest in G1 went through the subsequent S phase at a rate characteristic of the better medium, indicating that cells are not committed in G1 to an S phase of a particular duration.

Amino Acids↗
PubMed1984

[Correlation between cell cycle and cell morphology of RKN cells].

UNLABELLED: In order to study the changes in the morphology of each phase of the cell cycle, RKN cells, derived from a human ovarian myosarcoma, were synchronized by a mitotic selection method and studied under time-lapse cinematography, light microscopy, scanning and transmission electron microscopy. RESULTS: M-phase: The cells with relatively a few cytoplasmic organelles were small and spherical, and chromosome were seen in them. The cell surface was covered with numerous mivilli. Late G1,S and early G2 phase: The large, thin cells were flat and polygonal with various organelles inside and had central nuclei. Most of the chromatin patterns were finely granular. No microvilli were found on the cell surface. Early G1-phase: The paired daughter cells were fanshaped and the nuclei were eccentric with finely granular chromatin patterns. At the edges of the cells, rufflers which were related to cell movements were often seen. Late G2-phase: The thick cells were of a spindle shape and the chromatin patterns were a coarse granular type. Again on the cell surface microvilli increased and the slender filopodia were often seen.

Cell Cycle↗
PubMed2002

Influence of irradiation and pentoxifylline on histone H3 phosphorylation in human tumour cell lines.

Phosphorylation of histone H3 at Ser-10 correlates with chromatin condensation and this amino terminal modification is now recognized as a specific marker of mitosis. We have monitored the appearance of cells showing histone H3 phosphorylation in four human tumour cell lines to identify cell cycle progression after irradiation. In the human melanoma cell lines Be11 and MeWo and in the squamous cell carcinoma lines 4197 and 4451 a dose of 7 Gy of Co-gamma irradiation increases the number of cells binding anti-histone H3-P antibody 1-8-fold in a p53-independent manner. In the p53 mutant cell lines MeWo and 4451 H3-P phosphorylated cells can be detected as early as 30 min and show a maximum 1 h post-irradiation. In the cell lines Be11, 4197 and 4451 the early wave of H3 phosphorylated cells is followed by a second wave, which reaches a maximum 4.5-7 h post-irradiation and then declines. These events are attributed to damage-induced cell cycle blocks in the G1 and G2 phase of the cell cycle. Addition of the dose modifying drug pentoxifylline before irradiation increases the appearance of cells showing early and the late H3 phosphorylation. When pentoxifylline is added 12-24 h post-irradiation when the cell cycle blocks have reached their maximum the appearance of cells with phosphorylated H3 increases 3-5-fold in the p53 mutant cell lines MeWo and 4451. These observations are consistent with the function of the drug as a G2 block abrogator. The large H3 phosphorylation signal in p53 mutant cells is consistent with early entry of a cohort of G2 cells into mitosis. The smaller H3-P signal in p53 wild type cells correlates with the lower proportion of stable G2 populations in G1 blocked cells. These results indicate that pentoxifylline influences the appearance of histone H3 phosphorylated cells in a manner strongly dependent on the number of cells in G2 phase. This suggests that addition of pentoxifylline indeed abrogates the G2 block and thereby facilitates early entry into mitosis.

Histones↗
PubMed1988

Heterogeneity of insulin and insulin-like growth factor I binding in a human Burkitt type ALL cell line during the cell cycle and in three Burkitt type ALL sublines.

The expression of hormonal and growth factor receptors in leukemic cell lines might be heterogeneous due to the admixture of different cell cycle phases and the presence of yet unidentified sublines. Therefore, cell cycle-specific separation of Burkitt type ALL cells was performed by counterflow elutriation, and by limited dilution procedure three sublines of this cell line were obtained. Counterflow elutriation enriched to 60-80% purity for G1-, S-, and G2-phase which was shown by DNA flow cytometry. Insulin and insulin-like growth factor I (IGF-I) binding was investigated in the G1, S, and G2 phase. Insulin binding sites decreased from 10 to 15,000 per cell in G1 to 1,000-5,000 in S and increased to 40-50,000 in G2. The affinity of insulin binding remained constant during the cell cycle. IGF-I binding sites increased from 2,000 per cell in G1 to 5,000 in S and 15,000 in G2. The affinity of IGF-I binding decreased from G1 toward S and then remained constant in G2. The three isolated clonal sublines differed in numbers of insulin and IGF-I binding sites/cell without differences in affinity. The fact that IGF-I shows higher affinity binding during G1 than during S and G2 Burkitt type ALL cells suggests that IGF-I might be important for initiation of proliferation. The reduction in insulin binding sites during S-phase may indicate refractoriness of the cell to insulin during DNA replication.

Binding Sites↗